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Biomedical subjects

L Gorelkin

Publications and source records attributed to L Gorelkin.

29 records · Page 2Linked to original sources

Granular cell tumor of the abdominal wall musculature.

Granular cell tumor (myoblastoma) is a relatively frequent neoplasm found in many different anatomic locations. This is a case of such a tumor arising in the abdominal wall musculature, an extremely unusual site of occurrence. Excision with generous margins is required to prevent recurrence.

Abdominal Muscles↗

Epinephrine renal venography in severe inflammatory disease of the kidney.

In a comparative study of the diagnostic value of epinephrine renal venography (ERV) and angiography in eight patients with severe inflammatory disease of the kidneys, the spectrum of abnormalities exhibited by ERV was more striking than the angiographic findings. Complete disorganization of the renal venous architecture with linear streaking of contrast agent is a sign of renal inflammatory disease. ERV is a useful adjunctive diagnostic procedure in cases of a nonfunctioning kidney.

Adult↗

Fibroleiomyomatous hamartoma: a rare benign pulmonary "coin lesion".

A discussion of pulmonary hamartomas is presented along with a case presentation of a rare form, the fibroleiomyomatous variety. The need to differentiate these tumors from primary or even secondary malignant neoplasms always requires tissue diagnosis, necessitating surgical excision.

Hamartoma↗

Spindle cell lipoma: a benign lipoma variant with potential hazards of diagnostic misinterpretation.

Spindle cell lipoma is a relatively common, recently described benign lipoma variant. It demonstrates highly characteristic clinical and pathologic features. Knowledge of its existence and features should prevent any misinterpretation of its true benign biologic behavior, a pitfall which has unfortunately occurred in the past, resulting in poor prognosis and exaggerated modes of therapy.

Aged↗

Virus-induced pancreatic disease by Venezuelan encephalitis virus. Alterations in glucose tolerance and insulin release.

Viral infections have been implicated in the induction of diabetes mellitus in man and laboratory animals. Since virus-specific immunofluorescence (FA) is detectable in hamster pancreas during the acute phase of Venezuelan encephalitis (VE), experiments were designed to correlate pathologic and virologic events with metabolic studies in VE-infected hamsters. Golden Syrian hamsters were inoculated s.c. in groups of four to 12 with 100,000 plaque-forming units (PFU) of the vaccine strain (TC-83) of VE or 1,000 PFU of the virulent Trinidad strain of VE. Ultrastructurally, during Trinidad infection, mature virions were associated with the cell surfaces and within pancreatic beta cells in contrast to absence of virus-related changes in TC-83-infected hamsters. Virus-specific-FA was noted in islet cells and acinar cells of Trinidad-infected hamsters. VE growth curves demonstrated viral replication in pancreas with both strains. Although ultrastructural and FA changes were much more prominent in Trinidad-infected hamsters in contrast to TC-83-infected hamsters during the first few days of illness, the rapid lethality of the Trinidad-infected group necessitated performing all metabolic studies in TC-83-strain-infected hamsters. Accordingly, for the metabolic studies, glucose tolerance tests (GTT) using 2 mg. or 5 gm./kg. glucose i.p. were performed in groups of hamsters acutely infected two days earlier with the TC-83 vaccine strain and in 24-day and 90-day convalescent hamsters after TC-83 vaccine strain. Samples were obtained for glucose and immunoreactive insulin (IRI) determinations. Glucose intolerance occurred in hamsters in each of the infected groups given 5 gm./kg. glucose except for the 90-day convalescent TC-83 group. Severely decreased IRI responses occurred in the 24-day and 90-day convalescent TC-83 hamsters following both 2- and 5-gm./kg. glucose. Pancreatic IRI content in 24-day convalescent TC-83 hamsters was within normal limits, suggesting a defect in IRI release from the beta cells at this stage of convalescence.

Animals↗

Selective clearance of a benign clone of Venezuelan equine encephalitis virus from hamster plasma by hepatic reticuloendothelial cells.

A benign small-plaque clone of Venezuelan equine encephalitis virus was efficiently removed from the blood of inoculated hamsters by adsorption to cells of the hepatic reticuloendothelial system. More than 99% of infectious small-plaque virus, intrinsically labeled with 32P, was cleared from the blood within 30 min of inoculation; 47.6% of the 32P-labeled small-plaque virus inoculum was concentrated in the liver. In contrast, only 0.8% of a virulent large-plaque clone of the virus was cleared from the blood. The affinity of small-plaque virus for liver tissue was confirmed by electron microscopy, since inoculated small-plaque virions were readily visualized in phagocytic vacuoles of hepatic endothelial and Kupffer cells, where they appeared to be undergoing degradation. In contrast, large-plaque virus was not visualized in the liver. A critical determinant of virulence for viruses that do not replicate in hepatic reticuloendothelial cells may be the efficiency with which they are removed from the blood by adsorption to such cells.

Animals↗

Virus-initiated septic shock. Acute death of Venezuelan encephalitis virus-infected hamsters.

Hamster hematopoietic and lymphatic organs were studied sequentially by light and electron microscopy following Venezuelan encephalitis virus inoculation. In addition to extensive marrow and splenic necrosis nearly transmural necrosis of the ileum in Peyer's patch areas, with concomitant bacterial overgrowth, was noted. Viruses were observed ultrastructurally in reticular cells of Peyer's patches. In addition, bacterial blood cultures, consistent with an enteric origin, were generally positive in late stages of the infection. Reticuloendothelial function, measured by clearance of colloidal carbon, was significantly depressed in Venezuelan encephalitis virus-infected hamsters. It is proposed that the acute death of hamsters infected with Venezuelan encephalitis virus may be determined by the development of an endotoxic shock syndrome mediated by the extensive ileal lesions, coupled with impaired reticuloendothelial detoxifying function.

Animals↗

Pancreatic involvement by Venezuelan equine encephalomyelitis virus in the hamster.

Pancreatic tissue from hamsters inoculated with a virulent strain of Venezuelan equine encephalomyelitis virus (VEE) was studied sequentially with fluorescent antibody, light and electron microscopic technics. Progressive viral growth and cellular necrosis in the pancreas were demonstrated. Pancreatic infection resulted from both viremia and direct extension from the spleen across contaminated serosal planes. Mature viruses traversed the endothelium within endothelial vesicles and were associated with acinar as well as islet cells.

Animals↗

Venezuelan equine encephalomyelitis in an adult animal host. An electron microscopic study.

Adult white mice were inoculated intravenously with a virulent strain of Venzuelan equine encephalomyelitis virus. They were sacrificed sequentially, and cerebral tissue was collected for light and electron microscopic examination and virus titer determination. Viruses were first seen on the fifth day postinoculation infecting and arising from endothelial cells in the cerebrum. Subsequently, oligodendrocytes became infected, giving rise to mature virions. At this time in the infection, a particular electron-dense cell, probably representing a glial cell type, phagocytized mature virions. This resulted in autoinfection, as seen by viral growth in and destruction of these dense cells at a later stage of the infection.

Adult↗

Short-term in vitro culture and molecular analysis of the microsporidian, Enterocytozoon bieneusi.

The microsporidium, Enterocytozoon bieneusi, causes a severe, debilitating, chronic diarrhea in patients with the acquired immunodeficiency syndrome. Specific diagnosis of intestinal microsporidiosis, especially due to Enterocytozoon, is difficult and there is no known therapy that can completely eradicate this parasite. Preliminary studies indicate that a short term (about 6 months) in vitro culture of this parasite yielding low numbers of spores, may be established by inoculating human lung fibroblasts and/or monkey kidney cell cultures with duodenal aspirates and or biopsy from infected patients. The cultures may subsequently be used for the isolation and molecular analysis of parasite DNA.

AIDS-Related Opportunistic Infections↗